학술논문

Mouse cytomegalovirus-experienced ILC1s acquire a memory response dependent on the viral glycoprotein m12
Document Type
article
Source
Nature Immunology. 20(8)
Subject
Medical Microbiology
Biomedical and Clinical Sciences
Immunology
Infectious Diseases
Liver Disease
Prevention
Vaccine Related
Digestive Diseases
Biodefense
Emerging Infectious Diseases
1.1 Normal biological development and functioning
2.1 Biological and endogenous factors
Underpinning research
Aetiology
Infection
Inflammatory and immune system
Animals
Herpesviridae Infections
Immunity
Innate
Immunologic Memory
Interleukin-18 Receptor alpha Subunit
Liver
Lymphocytes
Membrane Glycoproteins
Mice
Muromegalovirus
Viral Envelope Proteins
Biochemistry and cell biology
Language
Abstract
Innate lymphoid cells (ILCs) are tissue-resident sentinels that are essential for early host protection from pathogens at initial sites of infection. However, whether pathogen-derived antigens directly modulate the responses of tissue-resident ILCs has remained unclear. In the present study, it was found that liver-resident type 1 ILCs (ILC1s) expanded locally and persisted after the resolution of infection with mouse cytomegalovirus (MCMV). ILC1s acquired stable transcriptional, epigenetic and phenotypic changes a month after the resolution of MCMV infection, and showed an enhanced protective effector response to secondary challenge with MCMV consistent with a memory lymphocyte response. Memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, and were independent of bystander activation by proinflammatory cytokines after heterologous infection. Thus, liver ILC1s acquire adaptive features in an MCMV-specific manner.